Evidence map›Paper›PMID 38277756›Full record

ArticleDrug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy2024

Inhibition of SIRT7 overcomes sorafenib acquired resistance by suppressing ERK1/2 phosphorylation via the DDX3X-mediated NLRP3 inflammasome in hepatocellular carcinoma.

Yuna Kim, Kwan-Young Jung, Yun Hak Kim, Pan Xu, Baeki E Kang, Yunju Jo, Navin Pandit, Jeongho Kwon, Karim Gariani, Joanna Gariani and 15 more

Open access · bronzeAbstract read
In one paragraph

Article in Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
7.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026
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  11. [Avitinib suppresses NLRP3 inflammasome activation and ameliorates septic shock in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  12. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

25 authors at 10 institutions in 4 countries.

Yuna KimDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea. Electronic address: yuna716@skku.edu.
Kwan-Young JungTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Daejeon, Republic of Korea.
Yun Hak KimDepartment of Anatomy, School of Medicine, Pusan National University, Yangsan, Republic of Korea; Department of Biomedical Informatics, School of Medicine, Pusan National University, Yangsan, Republic of Korea.
Pan XuLaboratory of Integrative Systems Physiology, Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne, Lausanne, Switzerland.
Baeki E KangDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea.
Yunju JoDepartment of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Navin PanditTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Daejeon, Republic of Korea.
Jeongho KwonDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea.
Karim GarianiService of Endocrinology, Diabetes, Nutrition and Therapeutic Patient Education, Geneva University Hospitals, Geneva, Switzerland.
Joanna GarianiDepartment of radiology, Hirslanden Grangettes Clinic, Geneva, Switzerland.
Junguee LeeDepartment of Pathology, Daejeon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Daejeon, Republic of Korea.
Jef VerbeekLaboratory of Hepatology, Department of Chronic Diseases and Metabolism (CHROMETA), KU Leuven, Belgium; Department of Gastroenterology and Hepatology, University Hospitals KU Leuven, Leuven, Belgium.
Seungyoon NamDepartment of Genome Medicine and Science, AI Convergence Center for Medical Science, Gachon Institute of Genome Medicine and Science, Gachon University Gil Medical Center, Gachon University College of Medicine, Incheon, Republic of Korea; Department of Health Sciences and Technology, Gachon Advanced Institute for Health Sciences and Technology (GAIHST), Republic of Korea.
Sung-Jin BaeDepartment of Molecular Biology and Immunology, Kosin University College of Medicine, Busan, Republic of Korea.
Ki-Tae HaDepartment of Korean Medical Science, Pusan National University School of Korean Medicine, Yangsan, Republic of Korea.
Hyon-Seung YiLaboratory of Endocrinology and Immune System, Chungnam National University School of Medicine, Daejeon, Republic of Korea.
Minho ShongResearch Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, Republic of Korea.
Kyun-Hwan KimDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea.
Doyoun KimTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Daejeon, Republic of Korea.
Hee Jung JungTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Daejeon, Republic of Korea.
Chang-Woo LeeDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea.
Kwang Rok KimTherapeutics & Biotechnology Division, Korea Research Institute of Chemical Technology, Daejeon, Republic of Korea. Electronic address: kkrok@krict.re.kr.
Kristina SchoonjansLaboratory of Integrative Systems Physiology, Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne, Lausanne, Switzerland. Electronic address: kristina.schoonjans@epfl.ch.
Johan AuwerxLaboratory of Integrative Systems Physiology, Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne, Lausanne, Switzerland. Electronic address: admin.auwerx@epfl.ch.
Dongryeol RyuDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea; Department of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea. Electronic address: dryu@gist.ac.kr.
Korea Research Institute of Chemical Technology · KRChungnam National University · KRGwangju Institute of Science and Technology · KRPusan National University · KRÉcole Polytechnique Fédérale de Lausanne · CHGachon University · KRHirslanden Clinique des Grangettes · CHUniversity Hospital of Geneva · CHKosin University · KRThe Catholic University of Korea Daejeon St. Mary's Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsSirtuin 7 (SIRT7) plays an important role in tumor development, and has been characterized as a potent regulator of cellular stress. However, the effect of SIRT7 on sorafenib acquired resistance remains unclear and a possible anti-tumor mechanism beyond this process in HCC has not been clarified. We examined the therapeutic potential of SIRT7 and determined whether it functions synergistically with sorafenib to overcome chemoresistance.

methodsCancer Genome Atlas-liver HCC data and unbiased gene set enrichment analyses were used to identify SIRT7 as a potential effector molecule in sorafenib acquired resistance. Two types of SIRT7 chemical inhibitors were developed to evaluate its therapeutic properties when synergized with sorafenib. Mass spectrometry was performed to discover a direct target of SIRT7, DDX3X, and DDX3X deacetylation levels and protein stability were explored. Moreover, an in vivo xenograft model was used to confirm anti-tumor effect of SIRT7 and DDX3X chemical inhibitors combined with sorafenib.

resultsSIRT7 inhibition mediated DDX3X depletion can re-sensitize acquired sorafenib resistance by disrupting NLRP3 inflammasome assembly, finally suppressing hyperactive ERK1/2 signaling in response to NLRP3 inflammasome-mediated IL-1β inhibition.

conclusionsSIRT7 is responsible for sorafenib acquired resistance, and its inhibition would be beneficial when combined with sorafenib by suppressing hyperactive pro-cell survival ERK1/2 signaling.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsSirtuinsCell Line, TumorCell ProliferationDEAD-box RNA HelicasesDrug Resistance, NeoplasmHumansInflammasomesMAP Kinase Signaling SystemNLR Family, Pyrin Domain-Containing 3 ProteinPhosphorylationSorafenibDDX3X protein, humanDEAD-box RNA HelicasesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinSIRT7 protein, humanSirtuinsSorafenibDDX3XERK1/2 phosphorylationHepatocellular carcinomaSIRT7 inhibitorSorafenib resistance

Identifiers

PMID38277756
PMCPMC10935544
OpenAlexW4390948824

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.